Abstract
We examined whether Aux/IAA proteins, key players in auxin-signal transduction, are involved in brassinosteroid (BR) responses. Iaa7/axr2-1 and iaa17/axr3-3 mutants showed aberrant BR sensitivity and aberrant BR-induced gene expression organ-dependently. Yokonolide B, which inhibits auxin signals by stabilizing native Aux/IAA proteins, inhibited BR responses. In contrast, the auxin antagonist p-Chlorophenoxyisobutyric acid did not inhibit BR responses. DNA microarray analysis revealed that 108 genes were up-regulated, while only eight genes were down-regulated in iaa7, suggesting that IAA7 functions not only as a transcriptional repressor but also as an activator. Among the genes that were up- or down-regulated in axr2, 22% were BL-inducible genes, 20% were auxin-inducible genes, and the majority were sensitive neither to BR nor to auxin. These results suggest that the Aux/IAA proteins function in auxin- and BR-signaling pathways, and that the IAA proteins function as the signaling components modulating BR sensitivity in manner dependent on organ type.
